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BCHE4130 W7 2 WCYL 2023 Revised

The document outlines the course schedule for BCHE4130 Molecular Endocrinology, detailing weekly topics such as hormones, glands, and endocrine disorders. It also discusses various endocrine disorders, their etiology, clinical manifestations, and treatment options. Additionally, it includes important announcements regarding quiz topics and assignment deadlines.

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0% found this document useful (0 votes)
18 views33 pages

BCHE4130 W7 2 WCYL 2023 Revised

The document outlines the course schedule for BCHE4130 Molecular Endocrinology, detailing weekly topics such as hormones, glands, and endocrine disorders. It also discusses various endocrine disorders, their etiology, clinical manifestations, and treatment options. Additionally, it includes important announcements regarding quiz topics and assignment deadlines.

Uploaded by

wongellen602
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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BCHE4130

Molecular
Endocrinology

Wilson Lau
Assistant Professor
School of Life Sciences
Course Schedule

The Molecular Basis of Hormones and Signal Transductions (W1)


The Hypothalamus and Anterior Pituitary Gland (W2)
The Thyroid Gland (W3)
The Adrenal Glands (W5)
The Islets of Langerhans, Diabetes Mellitus (W6)
The Gonads (W7)
The Hypothalamus and Posterior Pituitary Gland, Diseases of the Pituitary Gland (W8)
Student Oral Presentations (Mar 21) and Quiz (Mar 23) (W9)
Reproduction, Sex Hormones and Contraceptives (W10)
Steroid Hormones and their actions (W11)
Gastrointestinal (GI) Hormones (W12)
Calcium Homeostasis and Bone Metabolism (W13)

My email: wcylau@cuhk.edu.hk
Pituitary tumors and the optic chiasma
If a pituitary tumour develops and grows to such a size that
it pushes up into the hypothalamus above, it can disrupt the
optic nerve fibres crossing over in the optic chiasma. This
disruption would affect the fibres originating in the nasal
parts of the retinae of each eye, which receive light from
the temporal sections of the visual fields.

Loss of vision from the outer, temporal, visual fields

Bitemporal hemianopia (half-blindness affecting the two


temporal visual fields)

Optic chiasma comprises afferent nerve


fibres arising from the retinae of the eyes
Etiology of Endocrine Disorders / Diseases

Endocrine disorders occur from


- Hypersecretion-hyperfunction
- Hyposecretion-hypofunction
- Nonresponsiveness by target cells-hypofunction

Hypersecretion: secreting tumors, autoimmune diseases, or excessive


stimulation of the gland by trophic signals

Hyposecretion: failure or congenital absence of glandular tissue,


autoimmune destruction, surgical removal of the gland or lack of normal
trophic signals

Hyporesponsiveness: target tissue dysfunction; clinically similar to


hyposecretion (tissue resistance => downregulation of receptors)
Etiology of Endocrine Disorders / Diseases

Non-functioning
microadenomas
smaller than 6 mm are
present in up to 10%
Impaired
of normal population
development

e.g. Grave’s diseases

e.g. Sudden
removal of
glucocorticoids
Etiology of Endocrine Disorders / Diseases

Congenital
- Inborn genetic defect that causes excessive or deficient
production of hormone precursors

Autoimmune
- genetic predisposition and environmental trigger; reduction or
stimulation hormone response

Neoplastic
- hormones may be produced by abnormal tissue sites such as
malignancies
Etiology of Endocrine Disorders / Diseases

Functional disorders
- Caused by nonendocrine disease such as chronic renal failure,
liver disease, or heat failure

Tissue resistance
- Occurs when target tissue fails to respond to a hormone
(hormone resistance or target tissue resistance) (e.g. insulin)

Latrogenic
- Induced by medical treatments such as chemotherapy, radiation
therapy, or surgical removal of glands
- Treatment for endocrine hyperfunction involves removal or
destruction of glandular tissue => chronic hypofunction
- Chronic hormone replacement therapy may be required
Classification of Endocrine Disorders / Diseases

Primary, Secondary or Tertiary


- Since clinical manifestations are similar, lab test results are
required to distinguish them
Growth Hormone Disorders

- GH produced in anterior pituitary, regulated by hormone-releasing


hormone (factor) (GHR) and inhibited by somatostatin
- Primary target organ is liver
- Increases lean body mass, reduces fat mass, and induces liver to
release glucose under conditions of hypoglycemia

GH Deficiency
-Causes: brain tumor, radiation therapy, trauma to skull / sella
turcica

Clinical manifestations
- Short stature (dwarfism), hypoglycemia, tiredness, think hair,
poor nail growth, greater fat mass, decreased muscle mass,
delayed bone formation, delayed puberty
Growth Hormone Disorders

GH Excess
-Causes: uncontrolled GH production by somatotropic tumor

Clinical manifestations
- up-regulated growth of soft and bony tissues
- persistent hyperglycemia and increased insulin production
- Pituitary gigantism: occurs in childhood before the skeletal
epiphyses close (can reach heights up to 2 m or more)
- Acromegaly: occurs in adults, linear growth of bone is unlikely
but other tissues undergo hypertrophy
Growth Hormone Disorders
Growth Hormone Disorders
Thyroid Hormone Disorders

- Thyroid hormones, triiodothyronine (T3) and thyroxine (T4), are


regulated by TSH

- Thyroid hormones produced in follicular cells of thyroid


- regulators of metabolism; required for normal growth and
development of tissues

Hypothyroidism
- Causes: congential / acquired
- majority are primary, due to malfunction of the gland or
lack of development of the gland (underdevelopment of
nervous system, mental retardation)
- secondary, due to defects in TSH production (trauma,
tumors, radiation)
Thyroid Hormone Disorders

- most common cause of acquired hypothyroidism


=> lymphocytic thyroiditis
(Hashimoto disease or autoimmune thyroiditis)
(attach follicular cells of thyroid)
- irradiation of the thyroid gland
- surgical removal
- iodine deficiency
=> lack of T3, T4; stimulate TSH production
=> increased TSH causes thyroid cells to secrete
large amounts of thyroglobulin => goiter
Thyroid Hormone Disorders
Thyroid Hormone Disorders

Clinical manifestations of Hypothyroidism


- decreased basal metabolic rates
- weakness, cold intolerance, decreased appetite
- mild/moderate weight gain, slow heart rate
- elevated serum cholesterol and triglycides
- enlarged thyroid
- constipation
- depression / loss of memory or concentration (deficit in
neurological function)
- loss of eyebrow
- menstrual irregularity
Thyroid Hormone Disorders

Hyperthyroidism
- thyroid hyperfunction with increased synthesis/secretion of T4
and T3 (Graves disease)
- thyroid destruction (Hashimoto)

- primary – Graves disease (B cells make antibodies against TSH


receptors), autoimmune, tumor-related, inflammatory
- secondary – stimulation of TSH receptors by TSH
Thyroid Hormone Disorders
Exophthalmos
Thyroid Hormone Disorders

Hyperthyroidism
- Clinical manifestations
- insomnia, diarrhea, increased basal metabolic rate leads
weight loss, appetite intake increases
Adrenocortical Hormone Disorders

Adrenal cortex synthesizes


- Glucocorticoids
- Cortisol is the primary glucocorticoid
- Minearlocorticoids
- Androgens (sex hormones)

Adrenocortical insufficiency
- Primary: diseases of adrenal cortex, Addison disease, surgical
removal
- Secondary: inadequate secretion of ACTH
- Tertiary: hypothalamic injury

Cortisol insufficiency is most clinically relevant


Adrenocortical Hormone Disorders

Adrenocortical insufficiency
- Clinical manifestation
- tiredness, may only manifests with illness (stress/infection)
-weight loss,
- hypoglycemia, hyperkalemia (high blood potassium)
- anorexia
- low blood pressure, increased urine output, low blood volume

Addisonian crisis/acute adrenal insufficiency


- life-threatening, circulatory collapse
- may occur with acute withdrawal of corticosterioids
Adrenocortical Hormone Disorders

Hypercortisolism
- Cushing disease – pituitary hyperstimulation of adrenal cortex;
secretes excess cortisol
- Cushing syndrome – any other reason for hypercorisolism

Clinical manifestations
- loss of diurnal rhythm of cortisol secretion
- increase in appetite, weight gain
- increased in fat synthesis over protein, muscle weakness
- skin and wounds heal poorly, stretch marks
Adrenocortical Hormone Disorders
Adrenocortical Hormone Disorders
Gonadotrophin deficiency

LH and FSH deficiencies manifest in females with amenorrhoea due to lack of


ovarian secretion of oestrogen. In women older than 50, this may be confused
with the menopause, and the diagnosis is usually not made in older women. In
males, testosterone deficiency causes loss of libido and sometimes a reduction
in the growth of facial hair
- Treatment if necessary is by the administration of oestrogen in women
and testosterone in men
Hyperprolactinaemia
Prolactin is the only anterior pituitary hormone normally under tonic
inhibition from the hypothalamus. Whereas a pituitary tumour causes
deficiency of most anterior pituitary hormones, disconnection of the
pitu- itary gland from the hypothalamus by the growing tumour
causes a rise in circulating prolactin levels as the lactotrophs are no
longer inhibited by dopamine
- Prolactinomas (beign tumors of the lactotroph)
- causes galactorrhoea (spontaneous flow of milk from breast)
- also suppresses GnRH, causing amenorrhoea (absence of
menstruation)
- some men with breast hypertrophy, milk production
- testosterone deficiency, loss of libido
-treatment with dopamine agonsits
Antidiuretic Hormone Disorders
Antidiuretic Hormone Disorders
Alcohol also
inhibits ADH
release
Antidiuretic Hormone Disorders
Antidiuretic Hormone Disorders
Antidiuretic Hormone Disorders
Tips for the Quiz on March 23, 2023

The following topics will NOT be tested on the quiz,

Classification of endocrine pathologies


Hormone measurements and bioassays
Growth hormone
Prolactin f
Somatostatin
Thyroglobulin
Glucagon
Pancreatic Polypeptide
Announcement

Extension of deadline for the Assignment to March 20, 2023

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